The BIR2/BIR3-interacting Phospholipase D gamma 1 negatively regulates immunity in Arabidopsis

Plants have evolved effective strategies to defend themselves against pathogen invasion. Starting from the plasma membrane with the recognition of microbe-associated molecular patterns (MAMPs) via pattern recognition receptors, internal cellular signaling pathways are induced to ultimately fend off the attack. Phospholipase D (PLD) hydrolyzes membrane phospholipids to produce phosphatidic acid (PA), which has been proposed to play a second messenger role in immunity. The Arabidopsis PLD family consists of 12 members and for some a specific function in resistance towards a subset of pathogens has been shown. We demonstrate here that Arabidopsis PLD{gamma}1, but not its close homologs PLD{gamma}2 and PLD{gamma}3, is specifically involved in plant immunity. Genetic inactivation of PLD{gamma}1 resulted in increased resistance towards the virulent bacterium Pseudomonas syringae pv. tomato DC3000 and the necrotrophic fungus Botrytis cinerea. As pld{gamma}1 mutant plants responded with elevated levels of reactive oxygen species to MAMP-treatment, a negative regulatory function for this PLD isoform is proposed. Importantly, PA levels in pld{gamma}1 mutants were not affected compared to stressed wild-type plants, suggesting that alterations in PA levels are unlikely the cause for the enhanced immunity in the pld{gamma}1 line. Instead, the plasma-membrane-attached PLD{gamma}1 protein colocalized and associated with the receptor-like kinases BIR2 and BIR3, which are known negative regulators of pattern-triggered immunity. Moreover, complex formation of PLD{gamma}1 and BIR2 was further promoted upon MAMP-treatment. Hence, we propose that PLD{gamma}1 acts as a negative regulator of plant immune responses in complex with immunity-related proteins BIR2 and BIR3.\n\nOne-sentence summaryA phospholipase D is a novel negative regulator of plant immunity and forms complexes with regulatory receptor-like kinases.